Burns & Trauma最新文献

{"title":"Targeting Piezo1/2 ion channels for modulation of the lymphatic system: mechanisms, applications, and therapeutic prospects","authors":"Jingshu Wu, Xinxian Meng, Chengyao Han, Yuhao Sun, Ke Wen, Ke Li, Yixin Zhang, Xueqian Wang","doi":"10.1093/burnst/tkag048","DOIUrl":"https://doi.org/10.1093/burnst/tkag048","url":null,"abstract":"In recent years, the role of mechanosensation in lymphatic system development, functional homeostasis, and disease progression has received increasing attention. As key mechanosensitive receptors in lymphatic endothelial cells, Piezo1/2 ion channels respond to biomechanical stimuli such as fluid shear stress and interstitial pressure, thereby regulating calcium influx and downstream signalling pathways. These channels play pivotal roles in physiological processes, including lymphatic network formation, valve development, and the maintenance of meningeal lymphatic function. This review systematically describes the structural features and dynamic mechanisms of Piezo1/2 channels, with a particular focus on their biological functions within the lymphatic system. Piezo1 integrates multiple signalling pathways, including the Orai1/Notch, ANGPT/TIE/FOXO1, and EPHB4/RASA1 signalling pathways, to regulate lymphatic sprouting, valve morphogenesis, and meningeal lymphatic development. Dysregulation of Piezo1 function has been demonstrated to be closely associated with congenital lymphoedema, tumour lymphatic metastasis, and neurological disorders such as hydrocephalus and craniosynostosis. In addition, the potential role of Piezo2 in the sensory impairments associated with lymphoedema warrants attention. With respect to therapeutic strategies, this review comprehensively summarizes approaches targeting Piezo1/2, including the development of small-molecule agonists/inhibitors, gene-editing technologies, physical modulation methods, and advanced drug delivery systems, as well as their research progress and clinical prospects. Despite persistent challenges such as insufficient tissue specificity and limited spatiotemporal precision, the integration of multiscale biomechanical models, organoid platforms, and multidisciplinary research strategies holds promise for translational breakthroughs in Piezo1/2 ion channel research, providing a new paradigm for precision therapy of lymphatic system-related diseases.","PeriodicalId":9553,"journal":{"name":"Burns & Trauma","volume":"159 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148883544","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Microalgae: Emerging forces and prospects in the field of wound healing","authors":"Ruiyin Zeng, Haifeng Hu, Bobin Mi, Guohui Liu","doi":"10.1093/burnst/tkag060","DOIUrl":"https://doi.org/10.1093/burnst/tkag060","url":null,"abstract":"Viable microalgal cells have recently emerged as promising photosynthetic components of advanced wound healing systems because they can combine light-regulated oxygen generation, bioactive metabolite production, intrinsic imaging potential, and engineering flexibility within a single platform. In wounds with impaired or threatened healing such as burn wounds, traumatic full-thickness wounds, infected wounds, and chronic diabetic wounds, hypoxia, excessive inflammation, microbial burden, and impaired angiogenesis collectively hinder tissue repair and limit the efficacy of the currently employed therapies. In this review, the mechanistic basis and translational potential of microalgae in wound care is examined, with a focus on photosynthesis-driven oxygenation, antimicrobial and anti-inflammatory activities, antioxidant effects, immunomodulation, and bioimaging capability. We further summarize how viable microalgal cells or cell-derived products have been incorporated into hydrogels, three-dimensional bioprinted scaffolds, microneedles, electrospun matrices, coatings, and other biohybrid systems to achieve localized oxygen delivery, therapeutic molecule release, and multifunctional wound intervention. Importantly, we discuss the wound type-specific suitability of different microalgae-based platforms and critically compare them with existing oxygenation and antimicrobial strategies. We also highlight key barriers to clinical translation, including immune-mediated clearance, uncertain long-term survival and photosynthetic persistence in hostile wound microenvironments, limited light penetration, biosafety concerns, and challenges in manufacturing and standardization. Overall, microalgae-based wound therapeutics represent a highly promising but still early-stage strategy, and future progress will depend on mechanism-driven design, rigorous in vivo validation, and clinically relevant translational frameworks.","PeriodicalId":9553,"journal":{"name":"Burns & Trauma","volume":"349 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148877314","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Neutrophil–Epithelial Thbs1-CD36-JNK Axis Orchestrates Mucosal Barrier Failure in Intestinal Ischemia-Reperfusion","authors":"Yiwen Wang, Ran Li, Mengmeng Zhuang, Yuechen Fu, Qing Xu, Luqi Qiao, Simiao Chen, Jiayi Cao, Kehui Li, Ao Wang, Chao Meng, Wensheng Wang, Yong Sun","doi":"10.1093/burnst/tkag059","DOIUrl":"https://doi.org/10.1093/burnst/tkag059","url":null,"abstract":"Background Intestinal barrier failure following ischemia–reperfusion (IR) injury is a critical event that drives lethal systemic complications; however, the specific intercellular signals governing epithelial cell fate under these pathological conditions remain incompletely understood. Methods We performed single-cell RNA sequencing (scRNA-seq) on intestinal tissues from a murine IR model to map intercellular communication networks. The identified ligand–receptor pair was functionally validated using neutrophil-specific thrombospondin-1 (Thbs1) knockout mice, combined with pharmacological inhibition and activation of CD36, as well as biochemical and histological analyses. Results scRNA-seq analysis of the IR-injured gut revealed a key neutrophil–epithelial signaling pathway mediated by the Thbs1–CD36 ligand–receptor pair. Neutrophil-specific genetic ablation of Thbs1 markedly attenuated IR-induced epithelial apoptosis and barrier disruption. Mechanistically, Thbs1 binding to epithelial CD36 activated JNK signaling, mediating a proapoptotic cascade. CD36 inhibition was protective, whereas its activation bypassed the requirement for Thbs1 and provoked mucosal injury. Conclusions Our study elucidates a key mechanism of gut barrier failure and identifies the Thbs1–CD36–JNK axis as a promising therapeutic target for mitigating intestinal IR injury in critical conditions such as burns and shock.","PeriodicalId":9553,"journal":{"name":"Burns & Trauma","volume":"43 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148877328","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Roles and Regulatory Mechanisms of Autophagy in the Pathology of Spinal Cord Injury","authors":"Zhiwan Chen, Jiajun Deng, Ruijin Huang, Zhisheng Ji","doi":"10.1093/burnst/tkag058","DOIUrl":"https://doi.org/10.1093/burnst/tkag058","url":null,"abstract":"Spinal cord injury (SCI) remains a major clinical challenge due to its limited therapeutic options and the resulting severe functional impairments. Autophagy is an essential intracellular degradation process that plays a critical role in maintaining cellular homeostasis by degrading and recycling abnormal proteins and toxic substances. Recent studies have shown that autophagy significantly regulates several key pathological processes in the acute phase of SCI, including oxidative stress and neuroinflammation, and may also influence axonal regeneration during subsequent repair stages. Pharmacological modulation of autophagic flux has shown therapeutic promise and may exert neuroprotective effects. However, the precise relationship between autophagy activation or inhibition and functional recovery remains controversial and has not been fully elucidated. This review systematically summarizes recent advances in understanding the role and regulatory mechanisms of autophagy in the pathological processes of SCI, with particular emphasis on current controversies and unresolved issues. It also outlines potential pharmacological strategies targeting autophagy and proposes future research directions to support the clinical translation of these therapeutic approaches.","PeriodicalId":9553,"journal":{"name":"Burns & Trauma","volume":"209 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148852356","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Root-System-Inspired Core–Shell Microneedles Enable Spatiotemporal Sequential Therapy via ROS Scavenging, Angiogenesis, and Capillary-Driven Lipid Removal for Enhanced Fat Graft Survival","authors":"Hengyu Wu, Ganghua Yang, Yuanzheng Zhu, Yanglong Zhu, HaoWen Kang, Jiahui Wu, Minchen Zhang, Xinghong Zeng, Yangyan Yi","doi":"10.1093/burnst/tkag057","DOIUrl":"https://doi.org/10.1093/burnst/tkag057","url":null,"abstract":"Background Autologous fat grafting is widely used in reconstructive and aesthetic surgery, but its clinical outcomes are limited by early ischaemia–hypoxia, oxidative stress, delayed vascularization, and subsequent lipid accumulation-induced inflammation. Current therapeutic strategies generally focus on single-stage regulation and lack temporal coordination with the dynamic pathological evolution of transplanted adipose tissue. Here, we developed a root system-inspired core–shell microneedle platform capable of sequentially regulating the graft microenvironment through early vascular promotion and later lipid removal. Methods VEGF-loaded modified silk fibroin methacryloyl/grooved poly(lactic-co-glycolic acid) core–shell microneedles (VEGF@mSF/gPLGA-MNs) were fabricated by integrating a reactive oxygen species (ROS)-responsive mSF shell with a lipid-adsorbing gPLGA core. The physicochemical properties, ROS scavenging ability, VEGF release behaviour, and lipid adsorption capacity of the microneedles were systematically characterized. Their biological effects were evaluated using in vitro cellular assays and a mouse autologous fat grafting model. Graft survival, vascularization, inflammatory regulation, and adipose remodelling and the underlying molecular mechanisms were assessed by imaging, histological analyses, immunofluorescence staining, RNA sequencing, and Western blotting. Results The mSF shell rapidly responded to oxidative stress and degraded during the early stage after implantation, enabling localized VEGF release while alleviating ROS-induced cellular damage. Following shell degradation, the exposed gPLGA core facilitated directional lipid adsorption owing to its lipophilic properties and groove-mediated capillary transport. In vitro studies demonstrated improved endothelial migration, angiogenesis, ROS clearance, and mitochondrial protection. In a mouse fat graft model, VEGF@mSF/gPLGA-MNs significantly improved graft retention, reduced cystic degeneration and fibrosis, increased vascularization, and promoted adipose tissue remodelling. Transcriptomic and protein analyses revealed that lipid metabolism-related pathways, including PPAR signalling, were activated, and that inflammatory pathways, such as the NF-κB, TNF, IL-17, and Toll-like receptor signalling pathways, were suppressed. Conclusions The root system-inspired VEGF@mSF/gPLGA-MN platform enables spatiotemporally sequential regulation of the fat graft microenvironment by coordinating early vascular reconstruction with subsequent lipid clearance. This strategy provides a promising approach for improving fat graft survival and may offer a generalizable paradigm for regenerative therapies involving dynamic pathological transitions.","PeriodicalId":9553,"journal":{"name":"Burns & Trauma","volume":"6 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148806392","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bioadhesive Hydrogels as Immunomodulatory Interfaces for Chronic Wound Healing: From Microenvironmental Regulation Mechanism to Engineering Strategies","authors":"Kayoung Son,Soo A Kim,Minkyong Kang,Yejin Jo,Chansoo Kim,Kijun Park,Yunmin Jung,Tae Young Kim,Jungmok Seo","doi":"10.1093/burnst/tkag055","DOIUrl":"https://doi.org/10.1093/burnst/tkag055","url":null,"abstract":"Abstract Chronic wounds represent a major and growing clinical burden, particularly among ageing populations and individuals with diabetes, in whom persistent inflammation and immune dysregulation delay normal tissue repair. Addressing this challenge requires functional materials that do more than passively cover the wound and instead actively regulate the wound microenvironment. Advances in hydrogel chemistry and bioengineering have enabled the development of bioadhesive interfaces that maintain stable contact with wound tissue while modulating immune and regenerative responses. In this Review, we present bioadhesive hydrogels as immunomodulatory interfaces rather than simple wound coverings and systematically examine their mechanisms of action, including the reduction of microbial and inflammatory stimuli, modulation of macrophage polarization, regulation of NF-κB-, NLRP3-, and STAT-associated signaling, and control of mechanobiological signaling at the material–tissue interface. Through these mechanisms, bioadhesive hydrogels can alleviate excessive inflammation and support a regenerative microenvironment that promotes angiogenesis, re-epithelialization, and extracellular matrix (ECM) remodeling. We classify the engineering approaches used to achieve these functions into four complementary strategies. Structural and protective hydrogels stabilize the wound and protect it from contamination and mechanical disruption. Bioactive and regenerative systems deliver therapeutic molecules or cells to regulate inflammation and promote repair. Externally activated platforms provide spatiotemporal control over therapeutic activity, whereas sensing-integrated systems monitor wound conditions and support adaptive or closed-loop treatment. We also discuss major translational barriers, including unstable adhesion under exudative and mechanically dynamic conditions, limited long-term safety data, insufficient standardization, manufacturing challenges, and unclear regulatory pathways. Future progress will require disease-specific material design, clinically relevant validation, and the reliable integration of sensing and therapeutic functions.","PeriodicalId":9553,"journal":{"name":"Burns & Trauma","volume":"51 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148893898","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Xenium spatial transcriptomics identifies mesenchymal fibroblast expansion and conserved fibrotic ECM programs in keloid","authors":"Min Deng,Greogory M Brewer,Alejandro Espinoza,Julio Orellana-Montes,Keshvad Hedayatyanfard,Chanyue Hu,Md Golam Sarowar Jahan,Mojan Deriss,Jeremy C Davis,Carol E Cheng,Matteo Pellegrini,George W Agak","doi":"10.1093/burnst/tkag056","DOIUrl":"https://doi.org/10.1093/burnst/tkag056","url":null,"abstract":"","PeriodicalId":9553,"journal":{"name":"Burns & Trauma","volume":"22 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148894040","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Surgically Rebooting the Wound for a Healthier Operating System: Why the Apps Will Not Run Until You Reset the Wound Operating System","authors":"David G Armstrong,Alexandria A Armstrong,Lucian M Feraru,Wuquan Deng","doi":"10.1093/burnst/tkag053","DOIUrl":"https://doi.org/10.1093/burnst/tkag053","url":null,"abstract":"","PeriodicalId":9553,"journal":{"name":"Burns & Trauma","volume":"9 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148895697","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neuronal SPI1 suppression enhances axonal regeneration after spinal cord injury through Rassf10 downregulation","authors":"Dexia Kong, Roujia Kong, Yingying Yan, Haokun Zheng, Xiaowei Qian, Xu Chen, Yan Liu, Mei Liu, Ronghua Wu","doi":"10.1093/burnst/tkag054","DOIUrl":"https://doi.org/10.1093/burnst/tkag054","url":null,"abstract":"Background Axonal regeneration following spinal cord injury (SCI) is hindered by the intrinsic inhibitory properties of spinal neurons. While the role of the transcription factor SPI1 (PU.1) has been well established in myeloid cells, its function in neurons, particularly in regulating axonogenesis, remains poorly defined. The data from recent single-cell sequencing studies have indicated that SPI1 is clearly expressed in spinal neurons. Thus, we aimed to explore the effect of SPI1 on axonal growth and its underlying molecular mechanisms. Methods Primary cultured rat spinal neurons, CRISPR/Cas9-mediated spi1 mutation in zebrafish, and neuron-specific AAV9-shRNA delivery after rat spinal cord hemisection were utilized to manipulate SPI1 expression. RNA-seq, luciferase reporter assays, ChIP–qPCR, and Cut & Tag assays were employed to identify and validate Rassf10 as a candidate target gene of SPI1. Axonal outgrowth and functional recovery postinjury were assessed both in vitro and in vivo. Results Neuronal SPI1 expression declined progressively during spinal cord development but was markedly upregulated after SCI. SPI1 knockdown promoted axonal outgrowth, whereas SPI1 overexpression significantly reduced the axonal length. The transcriptomic analysis revealed that Rassf10 is a target gene of SPI1, which was subsequently validated by the results of luciferase reporter, ChIP–qPCR, and Cut & Tag assays. In vivo, spi1 mutation in zebrafish and neuron-specific SPI1 knockdown in rats facilitated axonal regeneration and functional recovery after SCI, as evidenced by significant increases in GAP43, NF200, and 5-HT expression and improved motor function compared with the control animals. The depletion of SPI1 or Rassf10 increased p-p38 MAPK levels and promoted axonal growth, whereas p38 inhibition abrogated these effects. Conclusions SPI1 impairs axonal growth and regrowth by transcriptionally activating Rassf10 expression, with this inhibitory effect mediated by the suppression of p38 MAPK signaling. These findings suggest that targeting the SPI1–Rassf10 pathway represents a promising therapeutic strategy for improving neural repair after SCI.","PeriodicalId":9553,"journal":{"name":"Burns & Trauma","volume":"29 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148726363","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Novel CAVIN1/GAS5 Axis Suppresses Skin Fibrosis through Mitochondrial Fission-Mediated Attenuation of the TGF-β/Smad Pathway","authors":"Hao Yang, Yuxi Zhou, Hailin Xu, Chengyan Huang, Shuting Li, Xiaohui Li, Xue Wang, Yongfei Chen, Peng Wang, Honglin Wu, Julin Xie, Jiayuan Zhu, Zhicheng Hu","doi":"10.1093/burnst/tkag052","DOIUrl":"https://doi.org/10.1093/burnst/tkag052","url":null,"abstract":"Background Keloids, which are characterized by excessive collagen deposition and fibroblast hyperactivation, present significant therapeutic challenges because of their high recurrence rates and incompletely understood pathogenesis. The transforming growth factor-β (TGF-β) pathway is a central driver, but its upstream regulators in the development of skin fibrosis remain elusive. Methods We integrated results of transcriptomic and proteomic analyses of patient-derived keloid and normal skin tissues. Functional validation was performed by using primary keloid fibroblasts (KFs) with gain- and loss-of-function approaches, RNA immunoprecipitation sequencing (RIP-seq), and actinomycin D chase assays. Two independent bleomycin-induced skin fibrosis mouse models were employed for in vivo validation. Results Multiomics profiling revealed that caveolae-associated protein 1 (CAVIN1) was consistently downregulated in keloids. CAVIN1 overexpression in KFs suppressed fibrotic phenotypes, including migration, invasion, collagen contraction, and ECM protein expression. Mechanistically, CAVIN1 directly bound to and stabilized the mitochondrial long noncoding RNA GAS5. This CAVIN1/GAS5 axis inhibited Drp1/Fis1-mediated mitochondrial fission and subsequent reactive oxygen species (ROS) production, leading to the attenuation of the canonical TGF-β/Smad2/3 signalling pathway. Critically, GAS5 silencing abrogated the antifibrotic effects of CAVIN1. Furthermore, database screening revealed that the histone deacetylase inhibitor vorinostat was a CAVIN1-upregulating compound. Both AAV-mediated CAVIN1 overexpression and vorinostat treatment significantly ameliorated skin fibrosis in the mouse models. Conclusions Our study reports a novel CAVIN1/GAS5 axis that concurrently targets mitochondrial fission and the TGF-β/Smad pathway to suppress skin fibrosis. These findings not only reveal a previously unrecognized mechanistic link in keloid pathogenesis but also identify CAVIN1 as a promising therapeutic target, with vorinostat as a potential repurposable drug for treating fibrotic skin disorders.","PeriodicalId":9553,"journal":{"name":"Burns & Trauma","volume":"3 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148703418","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}